HIV, in contrast to animal retroviruses, is not lysed by human serum but nevertheless the virus as well as virus-infected cells activate the complement system efficiently. HIV activates the classical pathway by binding C1q to the transmembrane protein gp41. On the surface of HIV-infected cells, both the alternative and the classical pathway are activated. Complement-treated HIV has an enhanced ability to infect cells carrying receptors for C3 fragments. By this mechanism complement can target the virus to certain cells, e.g. follicular dendritic cells. HIV-infected complement-coated cells can interact with complement receptor carrying cells and thereby spread the infection or cause the destruction of the infected cells. Due to direct or indirect effects of HIV the complement system is in an activated state and the cellular expression of complement receptors as well as regulatory molecules is modified in the blood of HIV-infected patients.
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